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NKp46 enhances type 1 innate lymphoid cell proliferation and function and anti-acute myeloid leukemia activity

It has been previously reported that the natural cytotoxic receptor NKp46 plays an important role in regulating natural killer (NK) cell biology. Here the authors show that NKp46 is required for the proliferation and cytotoxicity of type 1 innate lymphoid cells (ILCs) by activating the NF-κB signaling pathway and regulating IL-2Rα expression.

Rui Ma
Zhenlong Li
Jianhua Yu
ResearchOpen Access24 Jan 2025
Nature Communications

Volume: 16, P: 1-16
MYC functions as a switch for natural killer cell-mediated immune surveillance of lymphoid malignancies

Oncogene addiction is considered as a cancer cell-autonomous phenomenon, but can also influence the host immune system. Here the authors show that MYC-driven lymphomagenesis is associated with a block in the maturation and effector functions of natural killer cells as a mechanism of tumor escape from immunosurveillance.

Srividya Swaminathan
Aida S. Hansen
Dean W. Felsher
ResearchOpen Access05 Jun 2020
Nature Communications

Volume: 11, P: 1-17
Mechanisms of clonal evolution in childhood acute lymphoblastic leukemia

Secondary mutations can drive the transformation of pre-leukemic clones that carry ETV6-RUNX1 translocations. Müschen and colleagues show that repeated inflammatory episodes induce aberrant coexpression of the DNA recombinases RAG and AID to promote the development of acute lymphoblastic leukemia.

Srividya Swaminathan
Lars Klemm
Markus Müschen
Research18 May 2015
Nature Immunology

Volume: 16, P: 766-774
BACH2 mediates negative selection and p53-dependent tumor suppression at the pre-B cell receptor checkpoint

During B cell development, cells that fail to productively rearrange their immunoglobulin VH-DJH gene segments to generate an in-frame junction that codes for a functional pre-B cell receptor are deleted. Markus Müschen and colleagues now report that Bach2 is a key component of this pre-B cell receptor checkpoint that enables the elimination of normal and transformed B cells with nonfunctional V(D)J rearrangements by regulating the expression of p53.

Srividya Swaminathan
Chuanxin Huang
Markus Müschen
Research14 Jul 2013
Nature Medicine

Volume: 19, P: 1014-1022
BCL6 enables Ph⁺ acute lymphoblastic leukaemia cells to survive BCR–ABL1 kinase inhibition

Cihangir Duy
Christian Hurtz
Markus Müschen
Research18 May 2011
Nature

Volume: 473, P: 384-388
DYRK1A inhibition results in MYC and ERK activation rendering KMT2A-R acute lymphoblastic leukemia cells sensitive to BCL2 inhibition

V. S. S. Abhinav Ayyadevara
Gerald Wertheim
Christian Hurtz
ResearchOpen Access27 Mar 2025
Leukemia

Volume: 39, P: 1078-1089
Isoform-specific knockdown of long and intermediate prolactin receptors interferes with evolution of B-cell neoplasms

Malignant human B cells express autocrine prolactin (PRL), which has the potential to engage the long isoform and intermediate form of the PRL receptor to promote proliferation and/or survival.

Adeleh Taghi Khani
Anil Kumar
Srividya Swaminathan
ResearchOpen Access20 Mar 2023
Communications Biology

Volume: 6, P: 1-15
A mathematical model of tumor regression and recurrence after therapeutic oncogene inactivation

Sharon S. Hori
Ling Tong
Dean W. Felsher
ResearchOpen Access14 Jan 2021
Scientific Reports

Volume: 11, P: 1-14

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NKp46 enhances type 1 innate lymphoid cell proliferation and function and anti-acute myeloid leukemia activity

MYC functions as a switch for natural killer cell-mediated immune surveillance of lymphoid malignancies

Mechanisms of clonal evolution in childhood acute lymphoblastic leukemia

BACH2 mediates negative selection and p53-dependent tumor suppression at the pre-B cell receptor checkpoint

BCL6 enables Ph⁺ acute lymphoblastic leukaemia cells to survive BCR–ABL1 kinase inhibition

DYRK1A inhibition results in MYC and ERK activation rendering KMT2A-R acute lymphoblastic leukemia cells sensitive to BCL2 inhibition

Isoform-specific knockdown of long and intermediate prolactin receptors interferes with evolution of B-cell neoplasms

A mathematical model of tumor regression and recurrence after therapeutic oncogene inactivation

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